To: Cacaito who wrote (13918 ) 7/2/2000 1:20:50 PM From: Bluegreen Read Replies (1) | Respond to of 17367 Cacaito, WHAT AFFECT DOES NEUPREX HAVE ON HEPARIN????? It has been said that Neuprex might mop up endotoxin BUT what role as anti-inflammatory???? My opinion is that SYNERGY as an antibiotic is key. More RAPID and EFFECTIVE killing of GRAM NEG BUGS!!! But it has to be given IMMEDIATELY in order to have maximal effects. As far as cost.....NOT AN ISSUE. Just look at how many livers and kidneys are destroyed or damaged by administration of antibiotics for gram neg infections. Not to mention emergence of resistant bugs. Who is willing to take a chance when you have a safe addition to use???? Maybe even able to lower dosages of conventional antibiotics in gram neg infections and avert toxic dosages that are damaging to kidneys and livers not to mention hearing and eyesight damage. Once again I feel very confident in my investment now that we are mainly at this point in the hands of ALLERGAN, BAXTER and of course bigshot GENENTECH!!!!! Funny that the company you hate was picked by GENENTECH for anti-CD11a!!!! Unlike you who am I to second guess GENENTECH????? Only my opinions. You might want to think about this>>>>>>>>>>>>>>>Gut 2000 Jul;47(1):88-96 Related Articles, Books, LinkOut Heparin attenuates TNF-alpha induced inflammatory response through a CD11b dependent mechanism. Salas A, Sans M, Soriano A, Reverter JC, Anderson DC, Pique JM, Panes J Gastroenterology Department, Hospital Clinic, IDIBAPS, Barcelona, Spain. BACKGROUND: In addition to its anticoagulant properties, heparin has anti-inflammatory effects, the molecular and mechanistic bases of which are incompletely defined. AIMS: The current studies were designed to test the hypothesis that heparin abrogates the expression or function of leucocyte-endothelial adherence molecules which are fundamental to the acute inflammatory response. METHODS: The effects of heparin on tumour necrosis factor alpha (TNF-alpha) induced leucocyte rolling, adhesion, and migration as well as vascular permeability were assessed in rat mesenteric venules using intravital microscopy. Expression of adhesion molecules was quantitated using a double radiolabelled monoclonal antibody (mAb) binding technique in vivo (P-selectin, intercellular cell adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1)) or flow cytometry (CD11a, CD11b, and L-selectin). Ex vivo binding of heparin to neutrophils was assessed by flow cytometry. RESULTS: TNF-alpha induced a significant increase in leucocyte rolling, adhesion, and migration, and vascular permeability, coincident with a significant increase in expression of P-selectin, ICAM-1, and VCAM-1. Ex vivo assessment of blood neutrophils showed significant upregulation of CD11a and CD11b and significant downregulation of L-selectin within five hours of TNF-alpha administration. Heparin pretreatment significantly attenuated leucocyte rolling, adhesion, and migration but did not affect expression of cell adhesion molecules or vascular permeability elicited by TNF-alpha administration. Binding of heparin was significantly increased on blood neutrophils obtained five hours after TNF-alpha administration. Preincubation with an anti-CD11b mAb but not with an anti-CD11a or anti-L-selectin antibody significantly diminished heparin binding ex vivo. CONCLUSIONS: Our results support the concept that the anti-inflammatory effects of heparin involve attenuation of a CD11b dependent adherent mechanism.<<<<<<<<<<<<<